Low-carbohydrate diets increase LDL: debunking the myth

This week sees the publication of yet another study showing the superiority of the low-carbohydrate diet as compared to the low-fat diet. This study, published in the prestigious American Journal of Clinical Nutrition, demonstrates that subjects following the low-carb diet experience a decrease in triglyceride levels and an increase in HDL-cholesterol (HDL) levels; and that these changes are accompanied by a minor increase in LDL-cholesterol (LDL), which prompts the authors to issue a caveat.

Yes, although just about all the parameters that lipophobes worry about improved with the low-carb diet, the small increase in LDL has caused great concern and has prompted the authors to gravely announce that this small increase is troublesome and should be monitored closely in anyone who may be at risk for heart disease. Since most people who go on low-carb diets do so to deal with obesity issues, and since obesity is a risk factor for heart disease, it would appear that this small increase in LDL often seen in those following a low-carb diet could put these dieters at risk. Does it? We’ll see.

Let’s take a look at the study. But before we do, let’s digress for just a bit and look at low-carb diet studies in general.

As we’ve discussed in these pages before, there are a couple of ways to do dietary studies in which on diet is compared to another. You can compare a low-carb diet to a low-fat diet in a way that reflects what happens in real life. For example, you could randomize your study subjects into two groups, then give those in one group a low-carb diet book (Protein Power, maybe) and those in the other a low-fat diet book (an Ornish or McDougal book, perhaps). You would instruct both groups to follow their respective diets and come back periodically for evaluation. When these kinds of studies are done, the low-carb diet invariably brings about more weight loss and greater changes for the better in just about all parameters. But the folks who are proponents of low-fat diet cry foul. Why? Because in virtually all of these studies the subjects on the low-carb diet consume fewer calories than those on the low-fat diets. Lower-carb, higher-fat diets are satisfying, and it has been shown over and over that those following such diets actually consume fewer calories while still feeling full than do those following ad libitum (eat all you want) low-fat diets.

So, the low-fatters attribute all the improvement in those on the low-carb diets as simply a result of their lower caloric intake.

If you want to eliminate this caloric-deficit difference from your study, then you design a protocol in which calories are the same in both the low-carb and the low-fat arms of the study. This strays from the real-life way of looking at what is likely to happen when people buy diet books and follow them, but it does offer the advantage of getting rid of the calorie issue.

In these kinds of studies you randomize your subjects into either a low-carb or a low-fat diet group and put both groups on the same number of calories. At the end of your study, you can see the differences between the two diets – if any – that are brought about without calories being an issue.

The study under our consideration today is of the latter type; it’s one in which both groups were kept on an equal number of calories, a so-called isocaloric diet.

The researchers recruited 118 subjects who had abdominal obesity and at least one other metabolic syndrome risk factor and randomized them to either a low-carb or a low-fat diet for one year.

The diets were designed to be isocaloric with moderate energy restriction (≈6000 kJ/d [1433 kcal] for women, ≈7000 kJ/d [1672 kcal] for men). The planned macronutrient profile of the LC diet was 4% of total energy as carbohydrate, 35% as protein, 61% as total fat (20% saturated fat) with the objective to restrict carbohydrate intake to <20 g/d for the first 8 wk and to <40g/d (with the inclusion of an approved 20-g carbohydrate exchange) for the remainder of the study. The target profile for the LF diet was 46% of total energy as carbohydrate, 24% as protein, and 30% as total fat with the objective to restrict saturated fat intake to <10 g/d and <8% of total energy, with the inclusion of an approved food exchange (equivalent to the energy content of 20g of carbohydrate;) between weeks 9 and 52, so that the diets remained isocaloric.

Sixty nine subjects completed the study, and, fortunately, all the results reported in the paper were for the 69 completers, so we don’t have to worry about data contamination we would have gotten had the researchers done an intention-to-treat analysis. We know how the people fared who actually hung in there for the entire study period, which is what we want to know.

And how did they fare?

Those on the low-carb diet lost 26 percent more weight than those on the low-fat diet (14.5 kg vs 11.5 kg), but the difference wasn’t statistically significant. As you can see from the graph below of the weight loss between the two groups over time, the difference was widening, and we can extrapolate that the difference would have become statistically significant had the study gone on longer, but we can’t say for sure.

As for the other parameters, blood pressure, glucose, insulin, insulin resistance and C-reactive protein were the same for both groups. There was a difference in lipid outcomes, however.

The LC [low-carbohydrate] diet also provided greater improvements in triglycerides and HDL cholesterol than did the LF [low-fat] diet, which occurred independently of differences in energy intake and weight loss. This finding is consistent with those of long-term ad libitum studies. High triglyceride and low HDL-cholesterol concentrations are 2 of the MS risk factors, a syndrome that is associated with an increased risk of type 2 diabetes and CVD. Elevated triglyceride concentrations have also been identified as an independent CVD risk factor, and the triglyceride:HDL cholesterol ratio is considered a strong predictor of future cardiac events and is a surrogate measure of insulin resistance. Our data show that the triglyceride:HDL cholesterol ratio was halved after the LC diet and was approximately double the improvement observed with the LF diet. A recent review suggests that biological markers typically associated with the MS are those improved by carbohydrate restriction, which suggests that LC diets may offer the greatest clinical benefits for overweight populations who are insulin resistant and have several metabolic risk factors.

So far, so good. But now the other shoe is ready to drop.

Whereas the LC diet improved a range of cardiometabolic risk factors, greater increases in total and LDL cholesterol also occurred. Other studies that compared LC and LF diets reported similar findings, although the overall magnitude of the differences was smaller: 0.60 and 0.20 mmol/L in favor of the LF diet.

Let’s see how much the total cholesterol and LDL changed.

Those in the low-fat group started with an average total cholesterol of 212 mg/dl (5.5 mmol/L) and ended up a year later at same number. These same subjects also started out with average LDL levels of 131 mg/dl (3.4 mmol/L) and ended up the same at the end of the study. The low-carb dieters began the study with average total cholesterol levels of 209 mg/dl (5.4 mmol/L) and ended the study a year later with average total cholesterol levels of 232 mg/dl (6.0 mmol/L). Their average LDL levels started at 124 mg/dl (3.2 mmol/L) and ended up at 147 mg/dl (3.8 mmol/L).

The authors of this study bestow great significance on this fairly minor increase in LDL levels in those subjects on the low-carb diet. In their summary of the results of this study, they list the many benefits of the low-carb diet, then end on an ominous note:

However, these potential benefits may be counteracted by the detrimental effects of an increase in LDL cholesterol, which should be monitored…

The abstract of the study echoes this warning.

However, the increase in LDL cholesterol with the LC diet suggests that this measure should be monitored.

It was my impression that the tone of the authors was one of a little foreboding. Kind of a ‘this looks too good to be true, and, hey, look at those LDL levels; it is too good to be true’ aura about it. But is it too good to be true? Is the rise in LDL seen in most low-carb diets the hidden stinger? Is what all the lipophobes say true? You know, the old ‘Well you may lose weight on those diets, but you’ll clog your arteries at the same time.’

It’s all hogwash, of course, but before we get to the heart of the explanation as to why, let me remind you that numerous studies have shown that whenever subjects go on low-carb diets, they end up increasing the size of their LDL particles. Large, fluffy LDL particles are not only harmless, but may be protective. If they are protective, what’s wrong with having a bit more of them?

At the same time, numerous studies have shown that low-fat diets usually decrease LDL levels, but do so while reducing the particle size. Followers of such diets end up with lower levels of LDL made of smaller, denser, more atherogenic particles, which, in my mind, isn’t a good trade off.

The authors of our paper acknowledge this fact and cite some of this research, but they are still fixated – as are most lipophobes – on LDL levels. They just can’t get their heads around the notion that there is more to cardiovascular risk and health than LDL-cholesterol.

Since these researchers placed so much emphasis on LDL levels in their interpretation of all the data from their study, I got to wondering how they measured LDL levels. I looked in the Methods section of their paper and found the following:

The #11, of course, means that the description was in another paper that I had to go to the trouble of looking up. I always find it annoying when authors do this when they could just as easily stick a short paragraph in their paper and save people who really want to read it critically a lot of trouble.

Tracking down the other paper in the Journal of the American College of Cardiology, I found the following:

The LDL-C was calculated according to the method described by Friedewald et al.

What this means is that the researchers did not measure LDL levels directly in their study subjects, but calculated them using the Friedewald equation.

For reasons we don’t need to go into here, LDL is fairly difficult (as compared to total cholesterol and HDL) to measure. It can be done, but it’s expensive. So instead of measuring it directly, most labs calculate it based on an equation derived by William Friedewald and others in 1972.

Friedewald realized that it was pretty simple to measure total cholesterol, HDL-cholesterol and triglycerides. He knew that total cholesterol was the sum of all the various subfractions of cholesterol, which can be presented by the following equation:

Friedewald knew that it was easy to measure total cholesterol and HDL but difficult to measure the others. His insight was that the triglyceride level if divided by five could give a close approximation of VLDL. In running his experiments he also realized that this relationship held only if triglyceride levels were 400 mg/dl or under. If they were over this, all bets were off.

So, Friedewald substituted triglycerides (TGL) divided by 5 for VLDL in the above equations, giving us the so-called Friedewald equation for calculating LDL.

LDL = Total cholesterol – HDL – TGL/5

And this is how it is still done in labs all over the world 27 years after Friedewald’s paper. If you’ve had a lab report showing an LDL figure, I can guarantee it was calculated by the Freidewald equation and not measured directly.

What’s wrong with this if it works? Nothing. If it works. Problem is, it doesn’t always work. Friedewald himself found that in subjects with triglyceride levels greater than 400 mg/dl the equation didn’t hold. Anyone reading this who has had a lipid test showing triglycerides greater than 400 will have note on their lab report saying that LDL couldn’t be calculated because triglycerides were too high.

I’ve always thought the same held true for triglycerides under 100 mg/dl, which would apply to almost everyone who sticks to a low-carb diet for any length of time. Triglyceride levels of 40-90 mg/dl are not uncommon, and are, in fact, typical. When Friedewald did his work, the triglyceride levels were mainly up in the 150 – 250 mg/dl range, and in this range his equations match pretty well to directly measured LDL levels, but all bets are off with triglycerides above 400 mg/dl and, I suspect, triglyceride levels below 100 mg/dl. MD and I did find this ourselves in a few patients that we did direct LDL measurements on in our practice.

A paper published a few years ago in a pathology journal corroborating what we found. (Full text here.)

This paper is basically a case presentation of a 63-year-old man with a total cholesterol level of 263 (all results in mg/dl), an HDL of 85, a triglyceride level of 42, and an LDL level of 170. The LDL level was, of course, calculated using the Friedewald equation.

For some unexplained reason the authors of this paper decided to repeat the lab results and got the same readings. They then wondered if his very low triglyceride readings might be having an effect, so they measured his LDL levels directly and found that instead of the 170 predicted by the Freidewald equation, his actual LDL levels were only 126.

More recently a paper appeared in – of all places – the Archives of Iranian Medicine showing the same phenomenon. These authors tested 115 subjects with low triglyceride levels. You can get the full text of the paper, but a line in the abstract says it all:

The authors of this paper derived their own equation to be used in lieu of the Friedewald equation when the triglyceride levels are below 100 mg/dl. I suspect that if we were to apply this equation to the labs of the 33 subjects who finished the low-carb arm of the study we started out discussing in this post, whose average triglyceride levels were under 100, the LDL levels would have averaged much lower than the 147 mg/dl they were calculated to be by the Friedewald equation. If you subtract the 12.17 mg/dl that the Iranian paper estimates as the difference from the average triglycleride levels (an admittedly extremely unscientific and non-statistically valid way to do it), you find that the average drops to 135 mg/dl, which I doubt is significantly different than the 131 average of the low-fat dieters. If you did it the right way – subject by subject and then average – I suspect it would be greater yet.

The moral of this story is that if you have been following a low-carb diet and your triglycerides are low (or if your triglycerides are just low) and your LDL reading comes out a little high – or even a lot high, don’t let anyone mule you into going on a statin or undergoing any therapy for an elevated LDL. Demand to have a direct measurement of your LDL done. Or if you get an insurance physical and your triglycerides are low and your LDL up a little, fight to get a direct measurement so they don’t stick you with higher premiums because they think you’ve got an increased risk for heart disease.

What we do know based on the work of many is that low-carb diets change LDL particles to the large, fluffy, harmless variety. Thanks to these other papers we also know that the LDL levels so many people end up with on their lab reports after being on low-carb diets for a while are artificially high.

Now when you hear people say that low-carb diets may help you lose weight but run your LDL levels up and increase your risk for heart disease, you’ll know this is just so much gibberish. Sadly, your doctor will probably spout the same thing, and it will be up to you – who after reading this post will know more about this point than 99.9 percent of doctors practicing today – to educate your trained professional.

And if you are a researcher studying the effect of the low-carb diet on LDL, for crying out loud, hit your grant up for the extra few bucks it takes to get LDL cholesterol measured directly in your subjects so you won’t be in the embarassing position of having your data become worthless.

Geez, you’ve vaporized the last remaining shards of faith I had in metabolic science. All of this time I assumed people actually measured the things they reported, particularly if it is the one quantity they think is the most important. Silly me.

So if LDL is overestimated in those with low triglycerides, that means that VLDL is underestimated. After all, VLDL + LDL = Total – HDL, where the components of the right side are relatively easily measured, and the left side not.
Assuming the lipophobes realized that low triglycerides yields LDLs that do not fit the Friedewald equation, wouldn’t the next lipophobe tactic then be to decry the effects of high VLDL since it *is* a “bad cholesterol” as well as LDL?

It’s not that simple. Plus they’ve all got way too much invested in scaring us all with LDL. Besides, carbs cause the liver to put out VLDL, which is why triglycerides are a proxy.

Dr Eades,
Before discovering low carb, high protein and fat eating, I had the following values: T=214, HDL 44, LDL 153, TRI 101, VLDL 17 and then much to my “horror”, 6 months later on LC,
T=287, HDL 72, LDL 200, TRI 93, VLDL 16
The Med establishment hammers us about having a LDL of less than 130 and a Total/HDL ratio of less than 5 and as high as possible HDL and as low as possible TRI and a Total at around 200. It has all seemed so ambiguous and confusing.

Until I read your posting today, I thought maybe I was being lead astray by the low carbers because my low carb numbers seemed so out of whack from what I had been told by the establishment…..although I am feeling a whole lot better and losing weight and body fat.

Happiness is knowing that my LDL is made of a bunch of fluffy particles.

I hope that I am on the right track at an active age 66 to live a long and healthy life.

Dextery

I’m glad you can now breath a sigh of relief. BTW, I calculated your LDL based on the equation in the Iranian paper, and it came out to be 176 mg/dl, which is a lot lower than your calculated lab value of 200. Based on my experience this number usually falls as people stay on low-carb diets for the longer term.

An excellent post also teaching LDL calculation and its loopholes. Thanks a lot!

“As for the other parameters, blood pressure, glucose, insulin, insulin resistance and C-reactive protein were the same for both groups.”

I thought LC wins hands down in bringing down IR, plasma glucose, BP etc. There was also a paper extensively discussed in PPLP book which said insulin levels dropped by 46% on LC as compared to 8% on LF diet. What happened in this study?

LC usually always wins in short term studies, but sometimes in longer ones, too. You can find the full text of the study discussed in the PPLP here Just pull down the pdf.

As you can see, a huge jump in LDLs but also an improvement in Trigs & HDLs. Needless to say, it was a little disconcerting to see the jump in ‘bad’ cholesterol and the doctor poised to write a slip for statins.

Thanks for the post. It eases the mind slightly about the increase. I still need to find a somewhere that does direct measurement (in Australia) since the third blood test that was requested appears to be the same indirect measurement as the last two (despite requesting a measurement for particle size)

I calculated your LDL based on the equations in the Iranian paper and found your LDL to be 221 mg/dl, which is significantly lower than the calculated value. That, of course, assumes you made the conversions from mmol/l to mg/dl correctly.

Excuse my slightly off-topic question: I’ve heard hundreds of times that abdominal fat (which men tend toward) is more hazardous to health than fat in other places, say on the thighs or buttocks, but I’ve never heard the reason.

Is it a different kind of fat? Or is it solely its location that makes it dangerous? If so, why?

It’s a different kind of fat called visceral fat, and it’s very different from fat on the butt. It would take an entire post plus to go through all the difference.

Hi Dr E,
Dr William Davis has also covered this, particularly in the post “Making Dr. Friedewald an honest man”,http://heartscanblog.blogspot.com/2008/08/making-dr-friedewald-honest-man.html
He also covers the fact that patients can have exactly the same LDL, HDL and TG and TC, at least according to Friedewald, but have completely different clinical outcomes, because the Friedewald figures are screwed. (But I don’t have the time to dig out the posts.)
Cheers

I found significant changes after 6 weeks on LC, and more definitive results after 3 months. HDL: 42-49-54, TG: 214-93-101, ratio 5.5-4.6-4.6, fasting glucose: 77 at midpoint, down from high80s-mid90s over the past 4 years, LDL: 147-156-175. The rise in LDL was causing me concern until I read this article. I am waiting for results from a VAP. The one I had done 6 months ago put me well into the type ‘b’ range.

And if you are a researcher studying the effect of the low-carb diet on LDL, for crying out loud, hit your grant up for the extra few bucks it takes to get LDL cholesterol measured directly in your subjects so you won’t be in the embarassing position of having your data become worthless.

Not to sound too much like a conspiracy theorist, but maybe those “higher” LDL level results were the results the researchers wanted to see? The funders of the study’s website have traditional low fat info. But, maybe not, considering that 4% carb is good, rather than the 20-30% some studies try and pass off as low-carb.

Dr. Eades,
I further understand the calculation of LDL after your great post. Could you explain the method of direct LDL method? Is the LDL concentration in the blood measured for the direct measurement? Or is the direct LDL the same as the apoB count? Finally, a recent article in JAMA mentioned lipoprotein(a) and its correlation with increased MI, is lipoprotein(a) in a 1:1 relationship with a given LDL molecule and what are your thoughts on lipoprotein(a)?

Would appreciate your insight.

Thanks

Direct LDL measurement is just that: measurement of the amount of LDL in the blood. It isn’t calculated; it’s measured directly just as glucose is measured directly. It is not the same as the apoB, the apoB is a measure of a type of lipoprotein that kind of correlates with LDL levels, but isn’t the same.

Wow… yes thank you for the tips on how to get actual LDL measurements.
One thing though… these people only lost about 32 lbs with an entire year of very low carbohydrate and low calorie? Wouldn’t you think that these people who started out as obese would have their weights improved more? Obviously the lipid panel looks awesome (and that’s what really matters across the board), but what about their body fat percentages?

This always happens on these kinds of studies. Given the supposed caloric restriction, they should have lost a whole lot more, which tells me that they weren’t following the diet as prescribed.

Can I ask a question about fats? I took your advice and cut out all vegetable oils and have liked the results. It’s been pretty easy to do (if hand-making every morsel of food that goes into my mouth is easy), but summer is almost here, and, frankly, I want ranch dressing. And mayo for coleslaw (how can anyone low-carb without coleslaw?!). Is soybean oil inherently evil, or is it just the ratio of omega 3s to omega 6s that makes it bad. The mayo bottle at the store exclaims “rich in omega 3″! Homemade mayo made with grocery store olive oil tastes inherently evil. So I’m about to try making it with Grapeseed oil, but I’m not even sure why that would be better than soybean oil. Do you have any advice? Thanks again for all you do.

P.S. I enjoy your tweets. Hope it feels more respectable since twitter has prevented the Iranian Government’s desired media blackout. It is miraculous.

P.P.S. Unintended Global Warming Benefit: I heard a news report on a San Francisco radio station that some farmers are starting to feed their cattle a diet closer to grass-fed to cut down on all the gas emissions coming from their cattle. Ha!

MD makes all of our salad dressings, mayo and other things requiring a liquid oil with light olive oil. The taste of regular olive oil is a little strong for mayo, but light olive oil doesn’t have the strong taste. Give it a try.

You might be interested that two of the authors are not exactly impartial observers in this debate … and from the abstract at least, it doesn’t appear they have declared their interest.

Noakes and Clifton are responsible for the CSIRO “Total Wellbeing” diet books which caused quite a stir here a few years back, and I think still sell well, at least in part because the CSIRO is a well respected science institution. When the first of the books was launched this pair made a lot of disparaging remarks about Atkins and low carb generally (their diet is slightly lower carb, low fat, higher protein) – and also did battle with the anti meat protein brigade (their research had been funded by a livestock marketing authority).

Since that time there has been a certain amount of backtracking on the low carb front in research papers – eg;

Thanks for this post Dr Mike. I’ve been on a Paleo low carb diet for nearly three years now (because of grain intolerance and diabetes though I am slim, and always have been). My cholesterol profile has done just what you report and at the last test it was total cholesterol 6.6 mmol/L (255 mg/dl), HDL 2.4 mmol/L (93 mg/dl), Triglycerides 0.4 mmol/L (36 mg/dl) and LDL 4 mmol/L (154 mg/dl). Of course my endocrinologist has been trying, to persuade me to take a statin, unsuccessfully I might add, and I shall print off your post for my next check up with him in case he tries again. He’s actually very accommodating I’m glad to say, though he did tell me that he didn’t think it any use directly measuring LDL cholesterol or particle size so your post may come in very handy !

An added bonus of the Paleo low carb diet that I’ve discovered is that my teeth are much better. On a Neo diet, despite good brushing, I used to get build up of plaque and calculus on my teeth and needed a good clean from the dentist once a year – but now I don’t get any of this !

I have been following the low carb diet for quite some time now, especially after reading Protein Power. I’m not always as strict with it but I no longer take BP meds or medication for colitis and do not have any bouts of colitis so that is my gauge of how I’m doing.

Anyway, I had my first ever lab results where my total cholesterol and LDL were elevated. But, this also the first time my HDL were good, actually they got flagged as being high. Three years ago my HDL was 29. But here are the numbers from my labs taken 2 weeks ago:

Timely post for me, thanks! I lost 65lbs over a year ago now through mostly calorie restriction/semi starvation, poured off (realized later the best loss periods were when I ate low carb, but not by planning).

I bought Protein Power for 25 cents at a thrift shop (I’ve since bought everything Eades’ at the local book store) and read it on a lark. That was the beginning of true change for me. I am solid on my dietary regime now and have become a voracious reader of all things nutrition/exercise/lifestyle and love the info. I like to debate my nutritionist/medical trained friends and family! And I put it to practice.

I started a 90 day meat only challege to that end May 1 and had new blood work done to get info to compare after the 90 days is up Aug 1. Study of N=Me. My blood work immediately after semi starvation had me:

total 145, trig 38, hdl 69, ldl 68, vldl 8

after nearly a year on Protein Power, low carb, Paleo, etc I was at:

total 226, trig 34, hdl 82, ldl 137, vldl 7

and my doctor was “concerned and wanted to really monitor that LDL”, both numbers being calculated….. whatever, so I dug in and got myself educated on the cholesterol “thing” and have come to realize, at the age of 41, I am far happier to have HDL and total Chol UP, with the Triglycerides down even more. I’ll take 226 total over 145 total any day! Oh, and my C-reacitve Protein was measured at .3 low low low, so doubtful too much of that “bad stuff” is imbedding into my arteries.

First week of August I’ll be getting the full battery of tests again, just curious, but will spring for the NMR Lipoprofile to really nail down the particle type. Might as well see what 90 days of eating primarily local “wild” free range beef will have done to me. I am eating from the whole animal, marrow, brain, liver, kidney, heart, fat tissue for cooking in, the meat of course, just a nice grass fed cow. And I’ve been eating free range local eggs, plenty of wild trout, perch, and croppie, canned anchovies, herring, sardines, taking in lots of sunshine.

A recent dental visit had my dentist triple check his old slides of my teeth/jaw as he can clearly see increased enamel thickness and jaw bone density from 2 years previous to my weight loss and subsequent low carb living! Cool enough. He knows of Weston Price’s work, and sorta put it together a little based on that. But he still thought he’d pulled up the wrong xrays judging from my improvements!

A little more of my story here:

(page down to the cholesterol bit)

and here:

The Doctors Eaedes have truly improved and extended my life quality. Doubt I’ll live forever, but hey, maybe I can push it out there to a ripe old age in a robust manner.

My LDL always comes back a little high for my doctor but she doesn’t bug me about it anymore since I always mention the Freidwald equation, how I don’t think it holds up and if she wants to measure it directly then fine we can really get into it if she still wants me back on my statin. I quit that years ago and its apparently low enough for her not to want the fight as she knows I’ll come armed to the teeth and she won’t.

Unfortunately I ran into the problem you mention with life insurance. They jacked me with higher rate due to elevated cholesterol. After convincing my financial adviser to fight for a retest and find out what they numbers they actually considered (he was a former drug rep!), so I could alter the numbers for a retest. I didn’t think I could convince them about what really mattered. So I started taking extra doses of fish oil, etc. to get ready. They eventually just claimed they made a “mistake” and knocked me down into a healthier category and sent me check. I’ll wait till I lose more weight and then force them to give me a retest, which they say you can get and ask for a direct measure then.

“…who after reading this post will know more about this point than 99.9 percent of doctors practicing today – to educate your trained professional.”

Because you are a doc too, I feel a little reticent in making any negative comment about your brethren. But seeing that you also know that most docs are just ‘recipe followers’ heartens me. Sigh… I have met few, very, very few doctors (M.D.’s) that I could ever accuse of having a ‘scientific mind’. I have never, ever, ever, met a ‘naturopath’ that I could accuse of having one. ‘Woo’ , in fact, it is an accurate description of both sides of the allopath vs. naturopath argument in all but a very few cases.

ANYTHING that cannot be backed up by repeatable, falsifiable studies is ‘woo’ to me. (Most of the world is ‘woo’, I realize… “Woo! Look at those trees! Wonder where they came from!”) The moving target accusation about ‘homeopathy’ is certainly true, and it drives me nuts – why don’t homeopaths get together and round up some clients and design a double-blind test to present to the ‘establishment’. Their criticism about ‘each person is different and needs personal mixes’ may be valid (but I doubt it). It takes ‘years of study’ to accurately prescribe homeopathic substances. But I ask “Study of WHAT??” That I have never gotten any sort of answer to.

As was said in several posts you’ve made and several comments: “Most diseases tend to self-resolve”. Sure enough, if you have a cold, a bruise your ‘chakra’ is all screwed up or you have a ‘toxic’ colon – you take some ‘magic water’ . Woo! your cold gets better. Woo! your bruise goes away! Woo! Your ‘chakra’ is restored to ‘balance’. Woo! You are now ‘cleansed’ of ‘toxins’.

Having said all that, I will tell you that this serious skeptic lived with an herbalist in Vermont (Adele Godchaux Dawson – when I was there she was 78 years old, the daughter of a Cajun ‘witchdoctor’). She knew which herbs ‘did things’, and which ones were pretty ornaments in the garden. She got rid of my warts (I was thoroughly skeptical…) – when I showed them to her, she pulled up a plant just outside her door that she called ‘calf heart’, and it ‘bled’ some orange substance when the stems were broken. She rubbed some on the warts and told me to do so for the next 5 days. Within 10 days the warts had disappeared. However, she also believed in dowsing, crystal readings, saging for ghosts and seances and ‘future readings’. To which I did and still say “Woo!” Prove it!. (You have a 50/50, chance, more or less in guessing the ‘right’ sex of a baby – do it right and you have ‘magic’ and your ‘woo’ worth goes sky high! Do it wrong and if you are a ‘witch’, it is because the baby has ‘elements of the other’ so strong, that it blocked the actual ‘sex’ reading. Besides. ‘Sex’ is such an arbitrary assignment.. we are all just the same, right? On to the next.) Woo practitioners always have an excuse why something didn’t work and people fall for it repeatedly. (But so do M.D.’s largely… Always ready with the new prescription!)

Woo! Pretty good word Woo. But it should be applied to both sides of the argument when it is appropriate – pots should beware of calling kettles black!

I do go on, don’t I? I offer my thanks for the work you have put into pointing out the garbage that passes for ‘science’ and for extolling the good science that gets ignored by those that can only mindlessly follow recipes.

As always, I learn something new with each of your posts! That’s a pretty good hit rate!

However, on a humorous note – I can’t wait to see the look on the face of my Low-Fat Zealot Doctor if I have to tell him, “Oh, the LDLs aren’t really a problem – there aren’t too many of them, they’re just bigger and fluffier now. No worries.”

At least It’ll be more entertaining than the condescending “lecture” he gave me last year.

In Sept of 2008 I while taking Lipitor (20mg) and Zetia(10mg) I had muscle pain…cpk level was 500 or so. My doc took me off lipitor immediately and I began working out with more intensity and eating a healthy low carb diet…

The problem was my CPK was >50,000 at the time. I had full blow Rhabdo with renal failure. I had been working out a little harder prior to the test and really decided to kick it up a notch….then my arms were extremely sore and swollen. The workout did not include lifting weights, basically pushup and pulls up for an hour. I was admitted to the hosptial and put on IV. I was released after 3 days when cpk started to track back to normal.

My LDL size was tested and was described to me as “Pattern B” …small and dense. I’ve been faithfully following a very healthy low carb diet and have returned to working out lightly at first. The recovery from the Rhabdo has been improving… the neurologists have ruled out any underlying metabolic issue so far.

I won’t touch a statin again… I’m not sure what to do going forward. Are some people predisposed to high LDL from pure genetics? No amount of diet or workouts can keep the crazy high LDL in check?

Thanks for your time…

Tom

Rhabdomyolysis is a nightmare, and one of the side effects of statins that no one thinks about. Rhabdo is particularly a risk if taking a statin and a gemfibrozil or similar cholesterol-lowering agent.

I don’t know your definition of a ‘very healthy low carb diet,’ but my definition is very few carbs, a lot of fat and a moderate amount of protein.

do trig levels serve as a proxy for how tight your lo carb diet is? In other words, the lower your Trig level, you can essentially say that your lo-carbing is pretty tight?

I have a TRg of 20 and lo carb, but my LDL’s are small, and not large fluffy.

I don’t know how long you’ve been low-carbing or what kind of low-carb diet you’re following, but with triglycerides of 20, you should have a large LDL pattern. Maybe you should get another reading to make sure there wasn’t a lab error.

My 81-year old husband — slim, vigorous, still athletic, strong, and feeling great — was told two weeks ago by a cardiologist of vast reputation in our town, to begin taking a statin. Why? Because husband’s LDL was 77mg/dl! “A little bit higher than I like to see,” Famed Doc, said. (Whole picture: TC=170; HDL= 80; TRG=70; Ldl=77). Husband and I have been eating low-carb the Protein Power way for six years and we are both lean now and in excellent health. I was excited that my husband’s lipid profile was so good and could not believe the statin Rx he brought home that day. Over my dead body (an exclamation I don’t speak lightly at this age) will he take statins! Why would a physician give Lipitor to a healthy 81 year old, in any case, and particularly one with a lipid profile that I thought merited a gold star and kudos? No wonder you get so frustrated.

According to the Iranian equations, your husband’s LDL is 69, which should satisfy his cardiologist, who, I’m sure, hasn’t a clue about the Friedewald equation and low triglycerides.

I’ll say it again, even if your husband’s lipids were elevated, there is no data showing that statins would increase his longevity.

I have been reading this blog for some time now and have found it very informative. I have been following a high protein, low carb diet for some time now. I used to follow the Atkins diet and had very successful weight loss. I am very close to the end of weight loss (only 7 more lbs) and so have also needed to restrict my calories in order to continue with the weight loss. I have been having a couple of strange health issues, so I went to my Dr’s yesterday to have some testing done. I will not get into the health issues as it really does not apply to this post; she tested my urine and said I had a high amount of Ketone’s present. That did not suprise me. But then, she continued to explain to me how fatal this can be. She stated that over a long period of time (she considers that to be a few months) restricting my carbohydrates the way I do will create my blood to have high ph levels and can lead to a type of diabetic comma. She also stated how the brain only feeds off of glucose, and how by not supplying enough glucose to the brain this can create long term damage. This is the short version of the conversation; but the primary topic. I came back with my take on the diet, and much of the research I have done, and she flat out disagrees. I have to be honest; she definetly scared me. I am not going to change anything at the moment since I just had the blood work done and I will know the results by the end of the week; but this blood work does not check the acid level within my blood. Any thoughts?

Oh dear. Your doctor must have missed the med school biochem lectures on the day ketosis was taught. Assuming you’re not a type I diabetic, there is absolutely no way under the sun that you can go into a diabetic coma irrespective of what you eat or how high your ketones get. It’s impossible.

Read this post and you will understand vastly more than your doctor does about ketones and ketosis.

Good post – as always. Q: How do you know if your LDL was calculated or not? On a few of my physicals it doesn’t say anything next to the number or the type of lipid being tested. On a few it says ‘real’ next to the lipid tested and others say ‘direct.’

Hey Fred, looks like the real, directly measured LDL is the 165 one. If you run the total cholesterol, triglycerides and HDL through the Friedewald equation, you come up with 178 and change, which is the 179 number at the top of the list, so I suspect that is the calculated LDL.

Just for grins, I ran your numbers through the Iranian equation and came up with an LDL of 154, which is a little lower than the direct one. If that really is a directly measured LDL. They call it the ‘REAL’ LDL, but I don’t know what that means. Maybe the lab has an equation based on other factors that somehow modifies the Freidewald reading. I would check, just to make sure.

Any chance you could publish the formulas from the Iranian paper? I’d be curious to see what my LDL calculates on LC. When I went from a LF to a LC diet my numbers did this:

Low Fat:
Chol: 147 mg/dl
HDL: 19
LDL: 98
Trig: 120

Low Carb:
Chol: 187 mg/dl
HDL: 50
LDL: 127
Trig: 40

As I’ve said before, my doctor was EXTREMELY alarmed about the rise in total chol and LDL. I had to talk him off of the ledge by pointing out the HDL and Triglyceride improvements. It didn’t help.

Your LDL calculates to 95 mg/dl using the Iranian equation. I’ll be happy to put up the Iranian equation, but you can get the full text of the paper by going through the link I provided. Go to the pubmed page and look in the upper right area for a little box that takes you to the paper.

For readings in mg/dl (units used in the US) use this equation:

LDL = (total cholesterol/1.19 + triglycerides/1.9 – HDL/1.1) – 38

For readings in mmol/L (units used in Europe and the rest of the world)

LDL =(total cholesterol/1.19 + Triglycerides/0.81 – HDL/1.1) – 0.98

I wrote a little program on Excel so I can just plug in the values and generate the LDL levels. I’ve been having fun seeing how they come out.

One more regarding the statement,
“As for the other parameters, blood pressure, glucose, insulin, insulin resistance and C-reactive protein were the same for both groups.”

Your answer was
“LC usually always wins in short term studies, but sometimes in longer ones, too.”

I saw the previous post, but your answer didn’t seem to match the importance of LC in prevention of metabolic disorders. Insulin resistance and glucose levels (did they measure A1?) are two of the primary reasons to go LC. I’m surprised and somewhat concerned to hear you say that in long term studies LC “sometimes” improves these critical markers.

I say that because most of these studies (this one, for example) are populated with subjects recruited from newspaper ads who aren’t particularly motivated, especially not for the long term. As the study drags on both the low-fat and the low-carb arms tend to drift toward a more middle ground, which gives them the same long-term outcome. It’s different in short-term studies because the subjects are much more apt to stick rigidly with the protocol for four weeks or even eight weeks than they are for a full year. For this reason, in my opinion, you get much more valuable data from the shorter studies.

I have no connection with the company that makes the test, any labs that offer it, nor have I had it done, since I believe Malcolm Kendrick’s and Uffe Rasknov’s critiques of cholesterol as a marker of heart health.

A great test for a great price if you want to know your real verses calculated level of LDL and your LDL particle size. I don’t know how they can do it for this price.

I don’t know how long you’ve been low-carbing or what kind of low-carb diet you’re following, but with triglycerides of 20, you should have a large LDL pattern. Maybe you should get another reading to make sure there wasn’t a lab error.

THanks for your input; i think the NMR is probably correct; first one was in 2009 and TRG was 28; second NMR was in Feb of 2009, and was 20. Am going for another one again soon. Perhaps a change,but doubt it. I suspect it is genetic tendency given family heart disease picture. Oh, i am a slim male and weigh about 148. LO carb: meat, fish, vegs, some fruit. no wheat or starch or sugar, 2 tbs of ground flax. at times some hard cheese in small quantities. Diet has been pretty tight for over one year. Not sure i can tighten it up any more but am open to suggestions. Hard to imagine the diameter of the small LDL of 18.6 could increase to minimum of 20.5 to be considered large just by eliminating the flax and some metamucil give where the Trigs are.

This was a great post and probably applies to the overwhelming majority, but to all i would question. My particle count did come down since doing lo carb so that is at least a benefit!

Today, both you and Tom Naughton; over at Fat Head are talking about the same thing. http://www.fathead-movie.com/ I enjoy reading and respect the efforts of both yours and Mr. Naughton’s work.

The Fat Head post has this interesting bit of information…The most accurate measure of heart-disease risk is the ratio of triglycerides divided by HDL. The higher the ratio, the more likely you are producing small, dense LDL. Ideally, the ratio should be 2.0 or less. If it’s above 4.0, you’re in trouble. If it’s above 6.0, start putting your affairs in order.

I accept this statement and and by no means intend to argue it’s validity but Dr. Eades, I was wondering if you could explain a little further why this is the case. As you know. it’s difficult to get others to accept alternatives to the mainstream dogma. An solid explanation is always good ammunition when going into battle.

Thank you for your consideration.

Sincerely,

Chris

The idea that the triglyceride to HDL ratio is important comes from observational studies, so it isn’t all that reliable. We know that triglycerides go up with increased carb intake and we know that HDL goes up with increased fat intake. Therefore a low-carb diet (low in carbs, high in fat) should bring about a major improvement in this ratio. But we don’t know if it has anything to do with the trlglycerides and/or the HDL or if those values are simply markers for something else going on. Belt size is a marker for obesity, i.e., if your belt size goes up, you are becoming more obese. But the belt size doesn’t cause the obesity – it’s simply a marker. You can’t get rid of your obesity by simply buying a smaller belt. The same may hold for the triglyceride to HDL ratio – that may simply be a marker for something else that’s going in – insulin resistance, for instance. At this point we just don’t know.

Moderately Reduced Carbohydrate Diet Keeps People Feeling Full Longer
A modest reduction in the amount of carbohydrates eaten, without calorie restriction and weight loss, appears to increase a sense of fullness, which may help people eat less, a preliminary study found. The results were presented at The Endocrine Society’s 91st Annual Meeting in Washington, D.C.

“There has been great public interest in low-carbohydrate diets for weight loss, but they are difficult to maintain, in part because of the drastic reduction in carbohydrates”

Comment: Here’s a study that found carb reduction keeps you feeling full longer then states that drastically reducing carbs is difficult to maintain.

After two years on low-carb my total cholesterol went from 225 to 153, and while I don’t remember what my triglycerides were before they were only 51 when tested after the low carb years.

My LDL was up a little and the HDL down a little since the 225 test, and the doc busted on me for that a LOT more than he acknowledged the fact that I had dropped nearly 70 pts in total cholesterol (as well as 70 lbs!) while eating as much fat as I wanted. Unreal.

They can take their statins and stick ’em where the sun don’t shine ;).

Just a thought dashed off at work:
We haven’t had a Reckless Award for a while. And something never discussed with that looney Reckless perennial — the statination of the water supply — is, besides all the nasty side effects we know about, how stable is this stuff under heat? I mean, we also use the water supply as an ingredient for cooking (and for making beer, wine & spirits!!!!!!). Bet you anything that statins are not heat stable. (I’m guessing.) Besides the obscene amounts of money the drug companies will want — or is the statination going to happen after the drugs go generic? Just a thought.

I was interested in this comment in the abstract of this paper: “The LC diet may offer clinical benefits to obese persons with insulin resistance.” I’m too stingy to buy the full text.

Could you comment on this? I think it’s important that they admit that the LC diet may offer clinical benefit to what is an enormous percentage of those interested in diets.

Thanks.

I assume they’re talking about the improvement in triglycerides and HDL, which are markers for insulin resistance. The LC diet offered greater improvement in those parameters than did the LF diet. So, in their minds, the LC diet would be ideal for someone who is obese and has insulin resistance, but a little worrisome if that person had increased risk for heart disease (which of course said person would if he/she were obese and insulin resistant – both risk factors for heart disease) because of the slight increase in LDL, which is artificial since the LDL is calculated.

You are a well-kept man. But you have readily admitted this. I think the most beautiful thing on the planet may be couples that work so well together (at least the two of you appear that way). Aaah, and I found your lovely wife’s recipe for mayo. Should have looked there first. Thanks for your response and your eternally optimistic view that this is all do-able.

We don’t just appear that way, we really do work well together. It’s a perfect fit. Her strengths match my weaknesses and vice verse.

Mike,
Great post but slightly now confused about homocysteine levels on a VLCHF diet.In the comments by Malcohm Scott was a reference to study plublished by the Australian CSIRO’s
Noakes and Clifton and others. All the usual markers went down but homocysteine levels of
subjects on the VLCHF went up. Is increased homocysteine levels still a marker for heart disease or as long as the other markers are coming down, it dosn’t matter?

It’s still a marker and usually goes down on LC diets because of the increased vit B12. Don’t know what happened in the study you’re referring to, but sometimes you’ve got to balance things. If everything gets significantly better, but one supposed risk factor gets a little worse, does that mean you throw the whole thing out? I don’t think so.

In Protein Power Lifespan you refer to the high predictive power of the TG-to-HDL ratio with regard to heart attack risk. Do you still consider this a valuable criterion, or is there some newer, better set of parameters to use?

It’s still pretty good, but we don’t know if that the TG and HDL have anything to do with it directly or if they are simply markers for something else. See my answer to a previous comment on this same issue.

Look at who funded this study -that will tell you a lot. I’ve commented a number of times on this subject. Check here for the original and put ‘Reckless Award’ in the search function of the blog to see the others.

I’ve recently had a blood test that mimics the results above. I’ve lost 30 lbs of (primarily) abdominal fat in 6 months (dropped from 195 to 165 lbs), cut my TG in half, but saw my overall cholesterol “score” got from 195 to 217 due to increases in HDL (significant) and LDL (minor)

Anyway, since heart disease runs in my family, I’d like to minimize my risk factors. One widely touted method of decreasing cholesterol is to increase the fiber in your diet. Now, I’m not averse to fruits and veggies… but there are also products on the market now that claim to contain 10g of dietary fiber solely (it appears) through the use of polydextrose. I see mixed reviews of polydextrose – it’s good for the GI / bio-stuff, but not shown to have any impact on cholesterol.

I don’t think a total cholesterol of 217 is a risk factor. So why worry about it? The whole idea that cholesterol has anything to do with heart disease is simply an hypothesis – not a fact.

The reports I’ve seen on polydextrose show that it acts pretty much as a fiber. We use it from time to time for cooking, but not because of its fiber properties, but because polydextrose in combination with Reb A or sucralose mimics the cooking qualities of sugar without the sugar.

And, BTW, fiber itself is highly overrated. More and more studies are coming out showing it doesn’t do squat for much of anything other than increased regularity, and even that comes at a price.

As always, Mike, great dissection. In 2003, a paper published in Clinical Biochemistry (Volume 36, Issue 7, October 2003, Pages 499-504) showed the sames results as you presented them here, with respect to how misleading could be to use the Friedewald formula when TGs are either too low or too high. It explains all the reasons why the Friedewalf formula should not be used anymore, both from the practical point of view (prolonged fast, no chylomicrons in the sample, TGs within the formula’s range, etc) and from the scientific point of view as well. Moreover, it made the case for the adoption of directly measure apoB instead of calculating LDL to better assess a patient’s situation. That paper also discusses the rush in prescribing statins when the LDL number is high. I’m not sure if it shows in the aforementioned study’s references, but it seems to me like a must-have reference anytime the Friedewald formula is used.

The authors explain that one of their reviewers rose the issue of confusion if apoB would be adopted as the way to directly measure LDL: “Would introducing apoB into general clinical practice create confusion among patients and practitioners? Could the gains in diagnosis and therapy that cholesterol has brought about be squandered?” To which the authors offer that “it is not apoB that is complicated or confusing: it is cholesterol. There are now four different numbers that the physician must interpret and act on: Total Cholesterol, non-HDL cholesterol, calculated LDL and measured LDL”

Interestingly, the authors of the 2003 study end their discussion with something that since has resonated with me: “Could the public lose confidence in us if cholesterol is challenged as the central measure of the risk of cardiovascular disease? To ask this question is to answer it… Introducing apoB is small potatoes compared to introducing statins. With respect, the question is not how readily patients and practitioners will accept change, but how reluctant will the experts be”

The paper form Clinical Biochemistry was free to download when I did it back in 2003… unfortunately it not longer is but I could e-mail it should anyone be interested.

Thanks, Gabe. I hadn’t seen this. Didn’t come up in my PubMed search when I was looking for papers on the subject.

Dr Mike, I have read that high-protein, high-fat diets can lead to gout. Is this also a myth?

They can lead to gout only if they’re high-protein, high-fat, high-carb diets. If you remove the carbs, it isn’t true. We used the low-carb diet to treat gout in our practice, and it worked great. Gout isn’t something everyone is at risk for – only those with the genetic disposition. If you don’t have the genes for it, you can eat anything and everything and won’t get gout.

Is knowing whether low TG and high HDL are just markers for something else or good in themselves just a semantic question or does it mean we should not even try to lower TG and raise HDL? I understand the general principle that correlation is not causation, but when knowledge is limited, one has to tolerate some degree of inference short of absolute proof. It would seem to me that the constellation of facts about HDL and TG are more persuasive than “belt size causes obesity”.

I don’t put patients on low-carb diets to lower their triglycerides and raise their HDL. I put them (and myself) on such diets to improve overall health, well being, and to bring about weight loss. As a part of the process, the triglycerides go down and the HDL goes up. I don’t know if those changes are healthful in and of themselves or if they are simply markers of overall health, and I don’t really care. As far as I’m concerned the problem comes in trying to treat lab values as if they are themselves diseases.

Just want to mention again (I have posted this on other threads here) that until you actually test with something like the VAP you don’t know for sure if you have predominantly large fluffy LDL with the low triglycerides. I was so sure direct testing would prove to my doc that I had nothing to worry about, but instead the test showed I had much higher small dense LDL than was good.

Then I did a form of IF, called Fast-5, and my calculated small dense LDL went down to 314 ( optimal was listed as <600)

It may well be that long term really strict low carb would eventually lower the small dense LDL. My bet is that the longer you have been insulin resistant the longer it will take on just low carb to get the small LDL down. In which case, some form of IF would be worth a try.

Dr Eades,
I am looking for references demonstrating that the increase in LDL on a LC diet is large and fluffy. I’ve found this to be true for fish oil supplementation but can’t find references in any studies looking at low carb diets or saturated fat consumption. Please help.
Also a comment on the Iranian equation. There were two stipulations on the use of their modified friedenwald equation: trigs under 100, AND TOTAL CHOLESTEROL OVER 250. So if you apply their formula to someone’s labs where the TC is less than 250 the result may be innaccurately low. Therefore, unfortunately the 12.7 points you subtracted in the LC diet group’s results may also be an over correction. Not that it really matters.
Thanks for your help.

Don’t have the time to dig the studies out right now, but most are referenced in Gary Taubes’ book.

I’m a long-time reader of your blog (and books) but haven’t offered any comment for awhile. Just wanted to say that you’re still providing an excellent public service and I’m still reading the valuable info you provide. Also have continued to follow the PPLP regimen for more than two years now and it’s the best thing I ever did to improve and maintain health. Thanks again to you and M.D.

Best regards,

Wil

PS – Dr. William Davis who is another one of your readers has a terrific letter addressed to the WSJ on his blog, so I thought I would mention it to you and your other readers who may be interested. Here’s the link and the lede: http://heartscanblog.blogspot.com/

Thursday, June 25, 2009
The Myth of Prevention: Letter to the Wall Street Journal

Read the piece in the WSJ last Saturday and planned on posting on it myself. I agree with Dr. Davis letter.

In regards to gout, Charles Washington posted on his blog an unpublished chapter from GCBC that he got from Gary Taubes. The chapter is about gout research. Rick might find it interesting. It starts here:

Hi Dr. Mike. I left a comment earlier that ou responded to concering my Dr. stating that I run the risk of going into diabetic comma if I keep restricting my carb intake. I read your response and the link to the blog you left, and felt much relief afterwards. Today I got my blood results; the thyroid condition she thought I might have – negative. Not anemic, no lyme, good cholest. The bad news: she said normal blood sugar levels when fasting are between 65-100; I came in at 58. She say way too low. Vit. B12 normal range 200-1100; I came in at 252, but she wishes it were higher. Carbon dioxide levels normal range 21-33; I came in at 21. She says the carbon dioxide levels could be off due to if compensating for high acidic levels in my blood.

The original reasoning I went for testing mainly was because I missed my mentrual cycle for 5 months, my hair was breaking off severely, I get large bruises from what I don’t know, and I am tired all of the time. The only thing that I really changed was my diet. But I did a lc diet several years ago and did not experience this. This time around I also have been watching my calories since I have less to loose. I am 31 years old, 5″3, 117lbs. (goal 110lbs). I got off the phone with her today and she insisted that my problems are because I am not ingesting enough carbs. Now I am nervous. She will not test me for anything else. Do you think this could be possible?

There are no carbohydrate deficiency diseases. End of story. Go to any textbook of medicine used in any medical school in the country and try to look up carbohydrate deficiency diseases. There are none. There are fat deficiency diseases and protein deficiency diseases, but no carb deficiency diseases. Nature designed human physiology in such a way that we can make all the sugar we need, so we don’t really need to get any carbs at all.

If you are going to pay this physician to take care of you, please don’t run everything she says by me to check for accuracy. If you believe in her, then follow her instructions; if you don’t (and I assume you don’t otherwise you wouldn’t be checking with me), then ditch her and find someone else. Whatever you decide, I can’t be involved in this debate.

During Oct 2005, I sought to learn the difference in results between direct-measured lipids (using VAP) and the ‘standard’ lipid panel. Fasting blood was drawn by LabCorp at the same date and time. Here are the results (all values are mg/dL):

This morning I found in the papers a news item that was more or less presented as an attack on red meat consumption and that referred to a recent (23rd June) article in the BMJ. I tracked down the article: Trichopolou, A., Bamia, Ch. , Trichopoulos D. (2009), “Anatomy of Health Effects of Mediterranean Diet : Greek EPIC Prospective Cohort Study”, British Medical Journal, 338 b2337.

Here is the Abstract:

“Objective To investigate the relative importance of the individual components of the Mediterranean diet in generating the inverse association of increased adherence to this diet and overall mortality.

Design Prospective cohort study.

Setting Greek segment of the European Prospective Investigation into Cancer and nutrition (EPIC).

Participants 23 349 men and women, not previously diagnosed with cancer, coronary heart disease, or diabetes, with documented survival status until June 2008 and complete information on nutritional variables and important covariates at enrolment.

Main outcome measure: All cause mortality.

Results: After a mean follow-up of 8.5 years, 652 deaths from any cause had occurred among 12 694 participants with Mediterranean diet scores 0-4 and 423 among 10 655 participants with scores of 5 or more. Controlling for potential confounders, higher adherence to a Mediterranean diet was associated with a statistically significant reduction in total mortality (adjusted mortality ratio per two unit increase in score 0.864, 95% confidence interval 0.802 to 0.932). The contributions of the individual components of the Mediterranean diet to this association were moderate ethanol consumption 23.5%, low consumption of meat and meat products 16.6%, high vegetable consumption 16.2%, high fruit and nut consumption 11.2%, high monounsaturated to saturated lipid ratio 10.6%, and high legume consumption 9.7%. The contributions of high cereal consumption and low dairy consumption were minimal, whereas high fish and seafood consumption was associated with a non-significant increase in mortality ratio.

Conclusion: The dominant components of the Mediterranean diet score as a predictor of lower mortality are moderate consumption of ethanol, low consumption of meat and meat products, and high consumption of vegetables, fruits and nuts, olive oil, and legumes. Minimal contributions were found for cereals and dairy products, possibly because they are heterogeneous categories of foods with differential health effects, and for fish and seafood, the intake of which is low in this population.”

What struck me is that it doesn’t appear that the Mediterranean diet is here compared with a specific other diet. The comparison is between a higher Mediterranean and a lower Mediterranean diet (of whatever sort) and of the effect of specific elements of the diet.

Also, the low meat consumption in the diet is treated as a given and its effect is compared with that of the other ingredients of the diet, not with that of high meat consumption.

Do you know, doc, of any article directly comparing a LC diet with a Mediterranean diet as far as its effect on mortality is concerned?

There is NO study that legitimately demonstrates a reliable effect on mortality because all such studies are observational studies and aren’t worth a flip as far as determining causality. The only way you could legitimately do such a study and get valid results would be to randomize subjects into two groups, one of which followed the Mediterranean diet while the other followed the LC diet for life. You somehow make sure that each group is following the assigned diet – for life. You wait around until all the subjects are dead, then calculate which group had the greatest longevity. That’s the only way you can even remotely prove causality, and the reality is that it would take more than even this to do it. Ignore studies like the one you wrote about – they are worthless.

Thanks Doc, gonna print out & take to my endo next week when we discuss the results of my quarterly visit with the vampire in his office today. He insists on pushing statins tho my cardio doc backs me up when I insist statins have no benefit for women and further with the drops in my TC & TRI & LDL and rise in HDL even if the calculated LDL number is above the “acceptable” range is OK because I insist they are the large, fluffy type — he argues I can’t know that, then I insist he test…he says too expensive *sigh*.

Did you catch this article? http://eon.businesswire.com/portal/site/eon/permalink/?ndmViewId=news_view&newsId=20090622005507&newsLang=en titled “Expedition to Mount Everest Offers New Insights into Chronic Disease” (HIGHCARE2008) about using telmisartan to protect against the damages from hypoxia similar to that which occurs in those with apnea? Makes me wanna drop the Maxzide and go back on Cozaar IF if it has a similar effect ‘cept I still get occasional edema around my ankles for some unidentified reason (too much sodium?)*sigh*. If I drop the thiazide and am typical of other older women, I’lL be back to having normal BGs as long as I eat low carb (SHEP study); however, there’s that occasional edema thing. I still hafta drink low sodium V* and eat lots of parsley to keep potassium up & take 800 mgs magnesium citrate ’cause they both get flushed. Oh, the joys! I am practicing the first 2 steps ya gotta master before playing a digeridoo and discovered that I breathe so shallowly now that I can’t sustain the drone sound — interesting, I used to belly breathe, maybe the effect of nearly 2 yrs of CPAP…maybe not *G*.

Again, thanks for the ammo! I get so tired of educating my doctors; they’re the experts so why do I know more than they do about this stuff (rhethorical whine).

Wondering what you would say to a male patient who has some risk factors of heart disease but is well under the age of 65, say 50, and not yet diagnosed with heart disease – how do you know he won’t be diagnosed with heart disease by age 65, therefore putting him in that small percentage that might possibly be helped by statins. Even if this percentage was really only 20%, wouldn’t many men feel it was worth the risk? And as their doctor, would you?

The risk is vastly lower than 20 percent, and, no, I wouldn’t feel like it was worth the risk.

Sorry for posing more than one question – when you say your diet is low amount of carb, high amount of fat but just a moderate amount of protein – this indicates you are eating some foods that contain fat, nothing more – the only one I can think of that comes close is avocado. And I know you are not eating butter with a spoon… or are you. Is it the excess fat you might put on vegetables that makes the difference?

Re my previous comment – I was just curious to know if there was any circumstance at all in which you might compelled to use a statin.

I eat a lot of fatty meat; that’s the biggest part of my diet. The meat I eat contains more fat than protein calorically. And I often eat it with butter added.

I suppose there are circumstances in which I would put a patient on statins: If he/she held a gun to my head and threatened to pull the trigger unless I wrote the prescription. Actually, I might consider it in a male patient under the age of 65 who had been diagnosed with heart disease, but I would do so only after explaining all the ramifications, costs, side effects, etc., and the patient still wanted the drug.

I have been LC since last summer. I was strict for about 5 months, slacked a little bit for about 3 months and have been strict for the last 4. Yesterday I saw my doc to go over lab results compared to last year (the high FBG was the kick in the pants for me to make the permanent change to LC):

I was armed with knowledge from this post as I figured my triglycerides would be below 100 and it was possible that my LDL would be higher. As she told me the “grave news” and talking about the levels being close to medication time, I mentioned to her “well of course the LDL is calculated via the Friedewald equation which as we know does not work when triglycerides are over 400 and appear to over estimate them when they are under 100. But the good news is my HDL is going up and the triglycerides are going down which gives me a wonderful Triglyceride/HDL of 1.1 which is of course as we know WAY more important than the LDL or total choleserol. And the REALLY good news is my FBG has improved which means I am becoming less insulin resistant, awesome!” She looked at me blankly. She wants to check the levels again in 3-6 months.

As with several others posters here I was initially dismayed by the Total C and LDL being so high. I understand in your comments to other posters and in reading your books that as I continue LC, that number will drop. Perhaps you could post an article on time frames? I know each person is an individual and results will vary greatly so maybe it is not possible. It would be reassuring for many of to know that in another 6 months (or whatever) they will drift back down to a lower level. I am not sure if we check in 3 months if that is enough time.

Thanks for ALL you do!

Based on my experience, total and LDL-cholesterol levels fall with time, but even if yours don’t, what would you do? Go back on a low-fat diet to treat a lab value that has never been definitively shown to cause a problem? I would love to have been a fly on the wall when you gave your Friedewald didactic to your physician, whom, I’m sure, hadn’t a clue what you were talking about.

I want to share a nice joke I once read. It is in russian so I hope it doesnt lose a meaning in translation. Here it is! A young woman goes to a doctor and complains that her husband cant satisfy her. The doctor sais” Well, why dont you find yourslef a lover then? A woman replies” I did, and he doesnt hit the spot either” Well, sais a doctor why dont you find a second one? A woman sais ” I have four of them , and none can really satisfy me.” You know what”, sais the doc, you are very strange! Thanks God doctor sais the woman! Can you give me this diagnosis in writing that I am strange because everyone keeps saying I am a slut!!!!!

Well, this can be applied to the studies that keep finding low carb diet lacking. No matter how many of them are out there, none will ever satisyf those who refuse to be satisfied! Change the way you look at things and things you look at change!

Thanks, Ryan, for the link to the gout chapter, and thanks, Dr Mike, for answering my earlier question about gout.

Dr Mike, I must say I’m a bit uneasy about your attitude to observational studies. Doesn’t that in effect disparage most “traditional” knowledge, whether architectural (“If we build things in this way, they don’t seem to fall down”), medical (“People seem to recover from their fever when I give them this combination of herbs”), societal (“If we set up this kind of committee, things seem to function more or less peacefully and efficiently”)? I understand that an observational study doesn’t prove anything by itself but it seems that it’s a more formalized kind of traditional observation, one that, crucially, makes itself transparent and therefore open to future reinterpretation. I may be misunderstanding your stance, but I worry that in effect it negates most of humankind’s historical progress, and any kind of inquiry that doesn’t fit your preferred methods.

I have some sympathy with your question here. I’m in my 40’s and had a heart attack last year, and am now on statins (along with other medications and fish oil). It seems unlikely that statins have been beneficial to me now but would have been harmful up until the day before the heart attack. It seems reasonable to presume that there was some point in the last several years at which it would have been good for me to start taking a statin, along with blood-pressure-lowering medication. It occurs to me to wonder: Imagine an alternate reality in which I was put on a statin earlier, and I avoided a heart attack; how would anyone have known that I would have had a heart attack if I hadn’t been given the statin? I might well have gone into the figures as someone who had needlessly been put on a statin, thereby wasting money and risking all kinds of side effects.

Note that I don’t know how calculations such as “How many dollars does it cost to save a life by prescribing statins?” are performed so I may be getting this wrong. And one case clearly isn’t sufficient grounds to change a policy. But I do think that things might be a bit more complicated than Dr Eades suggests, and actually having a heart attack does make one a bit wary of (while simultaneously hopeful about) any approach that seems a bit radical. It also seems to me that widespread availability of heart scans of the sort recommended by Dr Davis could well solve the problem, by allowing anyone with multiple risk factors to see whether or not they are already suffering from atherosclerosis and need to get aggressive with the treatment.

Hi Doctor Mike, have been following your blog with great interest, thnx for such a great content! I have been eating pretty low-carb before, but lately cut the grains out and added much more fats. My new lab results did not sit well with my GP. From a totally normal cholesterol reading of total cholesterol of 198, I got the following:

My Doc was outraged with all my butter, coconut oil and fatty meet and eggs, and said this has to end or else…statins, inevitable CVD etc…hmmm.

I would appreciate your point of view, since this is all new to me and I although I already read enough to know better but a little reassurance from you would really help:-)))

Thnx in advance,
Kira

Using the Iranian equations, your LDL levels are 111 mg/dl, far below the 148 that has your doctor so concerned. You and your physician should be reassured by the HDL reading of 103. I’m constantly amazed at how ignorant physicians are about what lipid panels really mean.

My doctor, who in general is cool about my low carb diet, was “a little concerned” about my LDL. I said, “You know perfectly well that LDL is calculated by subtracting 1/5 of my triglycerides from my total cholesterol. I could lower my LDL by increasing my triglycerides…” She had the good grace to laugh and say, “Bad idea.” And admitted I was right.

On mayonnaise… I use high oleic sunflower oil. it has a similar fatty acid profile to olive oil without the strong taste of olive oil I used to use light olive oil until I found out that it is often cut with vegetable oils to increase the cost benefit.

As for the person asking for ranch dressing, you can easily make your own by mixing equal parts mayo, sour cream, and buttermilk. Add some garlic, chives, and parsley. You’re good to go.

As someone who possesses lots of large fluffy LDL (and few other markers of coronary problems), I hope you are right that large fluffy LDL are not atherogenic. That is not the universal view, however. James Otvos, the man who developed the NMR test for counting lipoprotein particles, wrote an article a few years back purporting to show by analysis of various studies that high particle count is atherogenic, whether the particles are large or small.

Here is the archive (thanks to the “wayback machine” web site; the paper had been taken down from its original web posting).

Doc, you seem pretty sure that large, “fluffy” (teddy bear?) LDL is, if not actually protective, at least benign. You suspect the PowerPoint presentation of Otvos’s talk at the ADA meeting is not at LipoScience’s site “because there was a problem with it.” OK, then here’s a journal article of which Otvos is one of 10 authors (Atherosclerosis 192 (2007) 211–217) which makes basically the same point: http://www.nypcvs.org/images/MESA.pdf

It seems to me that the only arguments for the differential atherogenicity of LDL by size are based on observational studies; that causal theories are as yet highly speculative; and that the thesis has become ubiquitous in the medical community in a way that is similar to the way that the conventional lipids view has become so orthodox.

LOL. I got déjà vous reading your response. I think I may have asked you that question before (if you would ever prescribe a statin) unless you have used that response before re another issue.

I have statins on my mind a lot lately. Besides my doctor trying to get me to go on them, I have a sister with bad side effects from them. She is convinced that if she stops she will have a stroke. Thanks for all the information you have so patiently provided.

I would consider it only in a male under the age of 65 who had been diagnosed with actual heart disease. Even then, I would have a long heart to heart with him before prescribing. I can truthfully say that I have never written a prescription for a statin in my life.

“Based on my experience, total and LDL-cholesterol levels fall with time, but even if yours don’t, what would you do?…”

After giving your question thought I am going to do 2 things.

1. Change doctors. Hopefully I can find one that understands blood lipids.

2. Stop testing the Total and calculated LDL cholesterol. Since they don’t mean anything there is no point in knowing what they are. All it will do is get doctors and insurance companies excited if they are high. I assume I can have just HDL and triglycerides tested separately as these DO mean something.

I will never take a statin, never go low fat, never give up low carb. Thanks for helping make my priorities clear for me.

right now I’m really glad I went back to read this post after I had ignored it for the past couple of weeks since it was up – I think I have yet to be disappointed after reading your blog. there’s just too much valuable information and it’s always entertaining to read. just wanted to mention that .) – and I’m actually hoping to get into a discussion about LC-diets and LDL-cholesterol sometime soon before I forget this stuff again…

the only downside is that it always makes me regret that I study political science…

For those who are worried about soy based mayo, and don’t want to attempt making it, there is a kosher product that you can get at organic food stores. It’s called “Hain” and it comes in two versions, canola oil or safflower oil. Pricey but worth it. The canola has a heavier taste, and neither has the light body of olive oil mayo but I find both to be tasty. The ingredient label lists all natural, whole products, something I haven’t seen in years on mainstream mayo labels.

I’ve read Weston Price’s info on soy based products and make a real effort to avoid it in anything I eat. I have since found that the packaged sausage I used to buy has soy flour, which it didn’t have a few years ago, and that restaurant breakfast sausages now have soy also. One can tell by the texture.

We are being slowly poisoned by the array of artificial and processed ingredients(soy, corn oil, HFCS and MSG put into mainstream products. Sometimes all these ingredients are found in one product(the packaged sausage)! There is a huge conflict of interest between the stockholder and the end user in so many corporations, not just food corps. and this is where we get the all-out attempt to substitute the cheapest ingredients in food products, consumer’s well-being be damned.

You’re right. Read a report the other day showing that 10 percent of calories in the American diet come from soybean oil and another report today that 17 percent come from sugar. Is it any wonder we’re having problems.

I wish you would write something on the “French Paradox”. A paradox is defined in the dictionary as: “A seemingly contradictory statement that may nonetheless be true” which in this case I guess it is but NOT for the reasons the low fat people believe. What caused me to think of this was an article on resveratrol which I just read. Resveratrol is contained in the skin of grapes which is supposedly the reason why the French don’t have the incidence of heart disease we have in the US even though they eat a high fat diet with lots of butters, fat and cream. The article I read states that they could not find enough resveratrol in wine to explain the “French Paradox.” Gee really? I wonder why?

In this case the paradox is only a paradox because the nimrods who named it that are lipophobes. They can’t understand why the French live longer and have less heart disease when they eat so much of that ol’ devil fat, so, to them, it is a paradox. To people who have good sense it isn’t a paradox; it’s the expected outcome.

This is very timely for me. My husband recently started eating low-carb (I’ve been low-carbing for years).

He is healthy, 33 yrs old, tall and skinny (6’2″ and 150lbs), but I’m convinced of the health benefits of low-carbing no matter what the weight, so we figured he’d give it a try.

He had to have his blood tested because he had an infection, so we took the opportunity to get his blood lipids tested too. He’s been seriously low-carb for about 3 or 4 weeks.

Before, his triglycerides were 103, his hdl was 36.3 and his ldl was 171.6

he just got his results back after the low-carbing, and is basically in a panic.

triglycerides are 72, hdl was 61.7 but ldl was 351!

so his triglycerides and hdl have improved, but his ldl has gone up almost 200 points in under 2 months (since the last test).

I remember reading that ldl can sometimes jump temporarily when starting low-carb, but that much? should we be concerned about this? or could it all be big and fluffy ldl so it doesn’t matter, or calculated wrong? is it possible this could be bad for him?

also – he actually lost weight in the past 3 weeks despite trying to eat lots of calories (in the form of protein and fat). he really cant’ afford to lose weight, he’s on the verge of underweight anyway. so how does he eat higher carb healthily?

thanks so much for your advice,

Deborah

Usually when I find something totally off base like this, I have the labwork redone just to be sure. Labs do make errors…often. So before I make any decisions about a really out-of-whack lab, I repeat it. Having said that, I have seen fairly dramatic elevations of LDL in a few people after starting low-carb. In the cases I have followed, it cleared up after a little time on the diet. I usually checked blood work on my patients every six weeks while they were actively under my care, so these high LDLs dropped by the 2nd 6 wk labs. When I have checked the particle size in these cases, it has always been of the big, fluffy variety.

Doc wasn’t sure you read this journal. The following is a sorta abstract posted on Reuters Health. Not bashing low carb but sure not endorsing its increased HDL effect. With the stated non-comliance how do they justify deriving any intelligent meaning from the data…just insane.

Clinical

No major advantage with low-fat vs low-carb diets in overweight diabetics

Last Updated: 2009-07-07 8:00:31 -0400 (Reuters Health)

NEW YORK (Reuters Health) – Overweight patients with type 2 diabetes who follow either a low-carbohydrate diet or a low-fat diet have similar outcomes after one year in terms of weight and hemoglobin A1C levels, according to results of a new study.

Dr. Nicola J. Davis of the Albert Einstein College of Medicine in Bronx, New York, and colleagues conducted the study in 105 adults with type 2 diabetes, body mass index (BMI) of 25 or more, and A1C levels between 6% and 11%.

Participants were randomized to a low-carb diet modeled after the Atkins diet or to a low-fat diet based on that in the Diabetes Prevention Program. They kept daily food diaries and were interviewed during study visits regarding their food intake in the previous 24 hours.

“The greatest reduction in weight and A1C occurred within the first 3 months,” the researchers report in the July issue of Diabetes Care. They note that “at 6 and 12 months, there was an increase in calories and macronutrients in both groups, suggesting decreased adherence.”

Although patients on the low-carb diet lost weight faster than those on the low-fat diet, after one year, both groups had “a similar 3.4% weight reduction” and neither group had a significant change in A1C level or blood pressure.

The low-carbohydrate group did have a significant improvement in mean HDL level (p=0.002).

The authors point out, however, that “the lack of change in A1C should…be taken in the context of reduced medications.” In fact, a third of subjects had been taking thiazolidinediones, which were stopped at the beginning of the study and not restarted. Furthermore, there was also a reduction in insulin and sulfonylurea dose overall.

“Perhaps we would have observed greater reductions in A1C if we did not make medication adjustments during the study; however, because we were concerned about hypoglycemia, not making adjustments would not have been appropriate,” the researchers comment.

I’ve been reading everything I could find about LDL today and came across your blog. Told today by a phone call (!!) that my recent blood work indicated the following levels:
Choles. 231 mg/dl
HDL 55 mg/dl
Tricyl. 88 mg/dl
LDL 158 mg/dl

Weight 129/ Height 5’4″/Age 48/Active, but not daily exercise due to work and graduate program

Told (stressing over phone again, by nurse!) that I needed to follow a strict diet to reduce LDL or I would be “put on meds”.

Current diet consists of chicken or fish each once a week, salads, vegetables, lots of fresh herbs, whole grain cereal/bread, fruits, tea, occasional snack of low fat cheese (mozzerella), low fat yogurt, lots of non-sweetened seltzer water, olive oil to cook; nothing ever fried, no chips, rarely eat out, but if I do….fish/salad. Willing to try stricter diet and committ to exercise over the summer, but did not like threat of meds without talking to me!!!

How can you be worried about the “threat of meds”? Are they going to hog you down, hold your nose, and force pills down your throat? It’s up to you whether or not you take whatever medications they recommend. Sounds to me as if your diet could do with a few less carbs. And your lipids look okay. Considering your low triglycerides, your LDL levels are actually lower than the test you got showed.

My doctor is concerned about my LDL but had nothing to say about the favorable HDL and triglyceride levels. Your explanation of what goes into an LDL calculation is a great comfort. So was losing 12 pounds.

Just to add my two cents: two months ago I turned up lipid values of the scary/shocking variety (TC: 544; HDL 123; Trig 59; LDL 409). On Dr Mike’s suggestion, I had a CT heart scan. Calcium score=zero. I also plan a VAP test for particle number/size which I’ll report when it comes in. I’ve never been concerned about heart disease (everyone in my family dies of cancer) but want to do my part anecdotaly to show the disconnect between LDL and disease.

I have a question which you already answered, but I just didn’t get it. If the LDL is really lower, then it must be that the VLDL is higher. why isn’t that by itself a problem? I’ll give you an example that I have just been working on. Total 242, HDL 59, Trigs 38. Based on the Friedewald equation the LDL is 175, while on the Iranian it’s 131. Adding the HDL 59 and the LDL 131, we are left with 52, what would that be? VLDL or IDL, both are supposed to be dangerous. And it would seem that the VLDL is even higher than the full trigs, not a fraction of it.

I really didn’t want my cholesterol levels checked, but since the Dr. put it on the lab requisition……
He is horrified at the numbers. I have to admit I was a bit taken aback myself.

Total 465
HDL 102.18
Trig 48.95
LDL 353.73

Even recalculating with the better formula leaves LDL really high. Given that I am a 54 year old female, very low blood pressure, no family history and very thin …… any reason for concern or further testing? Doc wants me to see a specialist.
Sigh. Ignorance was bliss….

I have asked for a blood test to directly test LDL particle size, but doesn’t sound like that is possible though the system I am in. All other indicators suggest low risk. Glucose is 80 (fasting). Given positive family Hx of heart bypass (father, age 60), my doctor strongly suggested a statin, to which I passed on. Your take?

I’m re-reading this particular blog in light of my new cholesterol readings. I’e been on a very low carb diet for three years now and my HDL cholesterol is always high and my triglycerides always low but my LDL has been rising and rising and rising over the three years. Today my measurements were: total cholesterol 7.1 (274), HDL 2.7 (104), triglycerides 0.5 (44) and LDL 4.2 (162) ! Using the modified Friedwalde calculation my LDL works out at a more respectable 3.1 (119).

My doctor is muttering about statins but knows I don’t want to take them. I do feel a bit concerned about the LDL though – why does it continue to rise, test after test ? When will it settle ? As I said, I’ve been low carbing (Paleo) for three years and I am slim, have never been overweight. The fats I eat are coconut oil and goosefat, I don’t eat polyunsaturated fats and rarely olive oil, only on salads.

Were I you and were I as worried as you seem to be, I would get the test that shows LDL particle size. If you’re LDL is going up but all the particles are large (as I suspect is happening), then that’s a good thing, not a bad thing.

I’d read a lot about cholesterol prior to getting these recent results–in GCBC, on this site, and in Mark Sisson’s website–and was still frightened by them and by my doctor’s attached note. Reading this post again was very reassuring, though I’d still like get a LDL particle size test to confirm that the particles are fluffy enough .

I’m trying to decide if I should should take up this argument with my doctor who is, by most other measures, a very good doctor, or abstain from this battle altogether and find a new PCP, especially since this issue is so central to a patient’s (i.e. my) well-being.

After following low carb my LDL had gone up and HDL had gone down, no density test was done but am i just not genetically disposed to follow this diet? At a young age I’m worried I’m hurting myself, I see all these success stories on blood work but mine had the opposite effect.
Confused??

I just had a Berkeley Heart Lab Test — they measure everything. Interesting stuff. Almost entirely positive. The highlights: I have the E4 Apo E genotype that predisposes me to inflammation (and, therefore, high cholesterol and a stronger reaction to fatty foods and even alcohol). I have slightly elevated LDL but the breakdown demonstrates that it is almost entirely made up of the harmless “fluffy cloud” LDL as opposed to the more dangerous dense, small particle LDL. Additionally, my C-Reactive Protein level is way way low, demonstrating that I have very little inflammation. And my triglycerides are low (which goes sky high on a high-carb, high-processed foods diet). My insulin level is, of course, very low, too. I eat a very low-carb diet, following the “paleo diet” about 75% of the time.

A while back someone asked about what to do about commercial mayonnaise, a hard to get away from ingredient in summer salads. Although I would like to make my own, I find I just don’t have the time on a regular basis, and even when I do, I’m not thrilled with the taste. I much prefer good ole’ Hellmanns, but wanting to get away from the awful oils they use, I finally settled on Wilderness Family Naturals Mayo (I don’t sell anything, have no connections to them or any other product). They list the following ingredients on their (glass) jar:

Dr Eades, Please help! I’m so confused! I’ve done the Atkins diet for years. I lost 45 lbs and felt great. Oh, by the way, I’m a 40 yr old wm. I’m a veteran. I go to the VA for my healthcare. Three months ago I had blood work done…TC-270, HDL-42, LDL-209, TRIG-91. Out of fear for my life, I abandoned my LC diet for a LF diet. Not to mention, I was put on a statin. I had blood work done again recently….TC-134, HDL-40, LDL- 81, TRIG-63. Most Doctors would be happy with those results. The problem is that I enjoyed LC diet and I could do it for life. This LF diet is torture! I’d kill for a steak right now! The VA doesn’t check particle size. I should add that I haven’t done the Atkins diet consistantly for years, rather off and on. Anyway, what should I do? Is the Atkins diet healthy for everone? Besides taking a statin, I also take Amlodipine and asthma meds. As you know, meds can drastically slow weight loss on Atkins. I felt more energenic on Atkins and didn’t need as much sleep. My instincts tell me to get off the statin and do low carb again. But I’m not a Dr. So what do I know? I would greatly appreciate your input. Thank you for your time.

Todd, I am new to this thread, did you continue the LF or switch back to the LC lifestyle? I am in a similar situation only reverse. I started out with “average” numbers while on a statin. I convinced my Dr to take me off of the statin and try LC. I lost weight, feel wonderful, my HDL improved, Trigs lowered, BUT LDL is 195 – direct measurement. I am wondering if I really need to go back on a statin and am trying to find out what is really going on and how bad is this. Thanks –

Of course, I panicked a bit at the TC/LDL number when I first got it but after much research and thought it seems perfectly consistent with what others have experienced, albeit pretty dramatic. Basically, a huge improvement in HDL, Tri, HDL/Tri and a stable TC/HDL even without the Iranian LDL adjustment which would bring it down in the area of 2.
LDL (Iranian). I assume, and will test sometime later, that my LDL particle size has increase substantially.

So, either I am a walking heart attack and need to run for the statins or I am one of the most metabolically healthy people around. My European doctor said the TC and LDL were “a bit high” but with this “constellation” it was nothing to worry about and the results “excellent.”

Jonathan – my most recent results in July after over three years of low carb and increasing TC, HDL, LDL but decreasing Triglycerides were:

TC = 294
HDL = 100
Tri = 35
LDL (calc) = 185
LDL (Iranian) = 135

My consultant (I live in the UK) wrote to my GP that my LDL was a bit “out of range for a diabetic” (I have atypical type 2 diabetes, am very thin and not insulin resistant) but that my ratios were good and that “she has actually calculated her LDL using a different formula and it is probably okay and I doubt that there is any major need to start a statin under these circumstances”

My husband and I changed to a Paleolithic-type diet Christmas Day 2010 after being on a vegan diet for about 9 months. The reason for the switch was health, as neither of us felt very good on the vegan diet, despite my expert cooking. We had to eat all of the time, and were low in energy. Neither of us has a weight problem at all. (He’s 6 feet 1 and weights only 150 pounds. I’m 5 feet 4 and weigh 115.) My husband’s total cholesterol was, however, only 140 on the vegan diet, and the doctor was delighted. We’re both 58.

It is now January 19, 2011. We’ve been doing the new diet for about 3-1/2 weeks, and he just had some blood work done due to the fact that his weight is so low. The doctor’s office just called saying that his total cholesterol was high and his “bad cholesterol” was too high. They told him that he should continue on a low-fat diet and consider medications.

I don’t have the numbers yet, but wondered if total cholesterol will jump up suddenly due to a change of diet like this and then settle back down as the body makes the switch?

I wanted to try the Paleo-type diet due to my auto-immune problem (celiac and alopecia universalis and psoriasis). Now, I feel like I’m killing my husband.

There is a phenomenon called ‘transient hypercholesterolemia’ that sometimes occurs when one begins a low-carb diet. The adipose cells contain cholesterol along with fat, and when the fat is released, the cholesterol is released along with it, causing a transient increase in cholesterol levels. These levels usually revert to normal in a few weeks. In your husband’s case, they may not, however, because his cholesterol level at 140 is probably too low. A number of studies have shown that there is risk of premature death with cholesterol levels that are too low as well as too high. As far as I’m concerned, the best number is significantly higher than 140.

Thank you very much, Dr. Eades. I continue to read and learn, and appreciate very much your expert view. We need to be ready when our doctor begins to talk medications. My husband takes no medications, and we’d like to keep it that way!

Given the results of my blood tests, I am very relieved to read this article. In terms of testing LDL particle size- is that done with a VAP? or what test do I request? I am going to request an actual ldl level be done.

I have been eating very low carb now for 2 years, and have also lost over 100#. However since last tested (maybe a year ago??) my ldl (and thus my total chol) have really jumped. When last tested all levels were “normal”- I believe “just” into the normal range.

Now my hdl has increased dramatically to 107 and my trg have decreased dramatically to 38; but this made my calculated my ldl at 172, pushing my total chol to 287. My numbers are not that different than the example given in the research study you referenced, so I’m assuming my actual ldl will be much less.

What do you think of Niaspan? I went LC about 18 months ago & my TC is now 348, HDL 87, TG 40 & calculated LDL of 247. I sanid no to statins, but agreed to start Niaspan of 500mg per day. I will be checked in mid August of 2011.

Way late to comment on this comment, but I don’t agree about the small meals. Basing solely on experience, I think you have to let your body get to the fat-burning stage. You have to do it by eating enough protein and fat to not be hungry, and go longer between meals. Also I have found the greatest weight loss to be when I went to bed at least two hours after my last meal, or went to bed just on the edge of being hungry, or, for me, below 100 blood sugar count. In the absence of insulin, another hormone comes out, the HSL, and unlocks the fat cells for huge stores of nutrients all night long for healing and the other metabolic processes. Go to bed hungry! (Not necessarily sober!) God designed us so well.

Thank you for this post. My blood test results literally had me crying this morning and this has helped me feel a little better. The message the doctor’s office left was simply that “your total and LDL are too high.” Hopefully my LDL really IS lower than the what it appeared to be! =)

I have been LC for 18 months.
My total cholesterol is 305, triglycerides 70, HDL 109 and LDL 189. The doctor retested my LDL and did a direct measurement and it came back at 195. She has been very supportive of my LC lifestyle but now we are both concerned about this LDL of 195. What do you think of this high number?

This is an excellent post. However, you could make it substantially more convincing by simply posting a comparison of some calculated versus actually measured LDL values. That is, simply take five low-carbers with low tryglycerides and have them draw blood and measure LDL in the two ways.

If LDL is shown to be lower with direct measurement, your case will be made very strongly. This would convince the non-believers.